1. Field of the Invention
The invention refers to a heart stimulator for stimulating at least a ventricle of a heart by means of electrical stimulation pulses in an overdrive stimulation mode wherein stimulation pulses to the ventricle are sought to be delivered prior to an intrinsic excitation of said ventricle. The invention particularly refers to implantable cardiac pacemakers and to implantable cardioverter/defibrillators (ICDs).
2. Description of the Related Art
Implantable heart stimulators can be used for treating a variety of heart disorders like bradycardia, tachycardia or fibrillation.
Depending on the disorder to be treated, such heart stimulator generates electrical stimulation pulses that are delivered to the heart tissue (myocardium) of a respective heart chamber according to an adequate timing regime. Delivery of stimulation pulses to the myocardium is usually achieved by means of an electrode lead that is electrically connected to a stimulation pulse generator inside a heart stimulator's housing and that carries a stimulation electrode in the region of its distal end. A stimulation pulse having strong enough a strength causes an excitation of the myocardium that in turn is followed by a contraction of the respective heart chamber. A stimulation pulse also is called a pace. Similarly, pacing a heart chamber means stimulating a heart chamber by delivery of a stimulation pulse.
In order to be able to sense a contraction of a heart chamber that naturally occurs without artificial stimulation (also called intrinsic contraction), the heart stimulator usually comprises at least one sensing stage that is connected to a sensing electrode on said electrode placed in the heart chamber. An intrinsic excitation of a heart chamber results in characteristic electrical potentials that can be picked up via the sensing electrode and that can be evaluated by the sensing stage in order to determine whether an intrinsic excitation—called: intrinsic event—has occurred.
Usually, a heart stimulator features separate stimulation generators for each heart chamber to be stimulated. Therefore, in a dual chamber pacemaker, usually an atrial and a ventricular stimulation pulse generator for generating atrial and ventricular stimulation pulses are provided. Delivery of an atrial or a ventricular stimulation pulse causing an artificial excitation of the atrium or the ventricle, respectively, is called an atrial stimulation event AP (atrial paced event) or a ventricular stimulation event VP (ventricular paced event), respectively.
Similarly, common heart stimulators feature separate sensing stages for each heart chamber to be of interest. In a dual chamber pacemaker usually two separate sensing stages, an atrial sensing stage and a ventricular sensing stage, are provided that are capable to detect intrinsic atrial events AS (atrial sensed event) or intrinsic ventricular events VS (ventricular sensed event), respectively.
As known in the art, separate sensing and pacing stages are provided for three-chamber (RA, RV, LV) or four-chamber (RA, LA, RV, LV) pacemakers or ICDs.
By means of a sensing stage for a heart chamber to be stimulated, the pacemaker is able to only trigger stimulation pulses when needed that is when no intrinsic excitation of the heart chamber occurs in time. Such mode of pacing a heart chamber is called demand mode. In the demand mode the pacemaker schedules an atrial or a ventricular escape interval that causes triggering of an atrial or ventricular stimulation pulse when the escape interval times out. Otherwise, if an intrinsic atrial or ventricular event is detected prior to time out of the respective atrial or ventricular escape interval, triggering of the atrial or ventricular stimulation pulse is inhibited.
Depending upon which chambers of heart are stimulated and which sense events are used different modes of stimulation become available. These modes of stimulation are commonly identified by a three letter code wherein the first letter identifies the chamber or chambers to be stimulated such as V for a ventricle to be stimulated, A for an atrium to be stimulated and D (dual) for both, ventricle and atrium to be stimulated. Similarly, the second letter characterizes the chamber or chambers sensed events may origin from (V: ventricle, A: atrium, D: ventricle and atrium). The third letter characterizes the mode of delivery of stimulation pulses: T=triggered, I=inhibited and D=dual (T+I). A fourth letter “R” may characterize a rate adaptive heart stimulator that comprises an activity sensor or some other means for determining the hemodynamic need of a patient in order to adapt the stimulation rate accordingly.
A dual chamber pacemaker featuring an atrial and a ventricular sensing stage and an atrial and a ventricular stimulation pulse generator can be operated in a number of stimulation modes like VVI, wherein atrial sense events are ignored and no atrial stimulation pulses are generated, but only ventricular stimulation pulses are delivered in a demand mode, AAI, wherein ventricular sense events are ignored and no ventricular stimulation pulses are generated, but only atrial stimulation pulses are delivered in a demand mode, or DDD, wherein both, atrial and ventricular stimulation pulses are delivered in a demand mode. In such DDD mode of pacing, ventricular stimulation pulses can be generated in synchrony with sensed intrinsic atrial events and thus in synchrony with an intrinsic atrial rate, wherein a ventricular stimulation pulse is scheduled to follow an intrinsic atrial contraction after an appropriate atrioventricular delay (AV-delay; AVD), thereby maintaining the hemodynamic benefit of atrioventricular synchrony.
By means of a ventricular sensing stage the heart stimulator is able to determine whether the heart undergoes a ventricular tachyarrhythmia that needs to be treated. Typically, a ventricular tachycardia (VT) is treated by way of overdrive pacing the ventricle with a stimulation rate that is higher than the intrinsic ventricular heart rate. Overdrive stimulation requires that the interval between consecutive ventricular stimulation pulses is shorter than an intrinsic (natural) VV-interval between consecutive ventricular excitations. The stimulation interval corresponding to an overdrive stimulation rate is called overdrive interval. The therapy using overdrive stimulation for treating a ventricular tachycardia is called anti tachycardia pacing ATP. ATP shall interrupt a ventricular tachycardia by interrupting a reentry cycle that oftentimes causes the tachycardia. If VT is not treated it may develop into life threatening ventricular fibrillation (VF).
For antitachycardia pacing (ATP), a VVI or a DDI mode of stimulation may be adequate. In such VVI or DDI mode, a ventricular stimulation pulse is not synchronized with a preceding atrial sense event (not “triggered” by an atrial sense event). In the VVI mode no atrial events are sensed nor are atrial stimulation pulses delivered. Only the ventricle is stimulated in a demand mode wherein ventricular stimulation pulses are inhibited if an intrinsic ventricular event is sensed prior to time out of a respective escape interval. In the DDI mode, both, atrium and ventricle, are stimulated in a demand mode wherein atrial or ventricular stimulation pulses are inhibited if an intrinsic atrial or ventricular event is sensed prior to time out of a respective escape interval.
The concept of ATP is based on the observation that VT often involves reentry, which usually has an excitation gap between the leading edge of excitation wavefront and the trail of refractoriness. By delivery a critically timed premature stimulation pulse (or train of stimulation pulses), ATP may pre-excite the excitation gap and disrupt the reentry circle. With improper timing, the ATP may miss the excitation gap and cannot terminate the reentrant rhythm.
Timing of stimulation pulses therefore is crucial. When stimulating a heart with an overdrive stimulation rate, it is attempted to deliver a (premature) stimulation pulse prior to a possible intrinsic excitation and thus render a respective heart chamber refractory so it is not susceptible to any further (natural) excitation during a (natural) refractory period needed by the cells of the myocardium to repolarize and thus become susceptible for further excitation again. However, too early a stimulation pulse would either be ineffective because the myocardium is still refractory (that is not susceptible to intrinsic or stimulated excitation because the myocardium is still depolarized) or, even worse, could meet the vulnerable phase of the myocardium, bearing a high potential risk of inducing a ventricular fibrillation that is worse than tachycardia to be treated. During the vulnerable phase the myocardium has only partially repolarized.
In a heart cycle, an excitation of the myocardium leads to depolarization of the myocardium that causes a contraction of the heart chamber. If the myocardium is fully depolarized it is unsusceptible for further excitation and thus refractory. Thereafter, the myocardium repolarizes and thus relaxes and the heart chamber is expanding again. In a typical electrogram (EGM) depolarization of the ventricle corresponds to an R-wave. The vulnerable phase of the ventricular myocardium coincides with the T-wave.
If the pacing pulses happen to coincide with the vulnerable period (VP), which is defined as a critical time window around the peak of T wave in surface ECG, the ATP are prone to induce fast or unstable VT. This is the well-known “R-on-T” phenomenon.
Despite different ATP algorithms (burst, ramp, scanning, etc), most ICDs are programmed to deliver ATP pulses with slightly shorter cycle length than that of the detected VT, based on predefined cycle percentage or step decrement. So far, there has been no consensus on “optimal” ATP timing parameters. In clinical practice, the setting of ATP timing parameters in ICDs is arbitrary or based on experience. As a result, current ATP algorithms have intrinsic risk of inducing VT/VF, because these algorithms are not designed to prevent the incidence of R-on-T events. In other words, there are intrinsic risks that ATP pulses are delivered during the ventricular VP.
Current ATP algorithms can only effectively terminate about 80 to 95% of spontaneous episodes of slow VT, and is not recommended to treat fast VT or VF. It is also observed that the present ATP algorithms have potential risk (ranging from 2% to nearly 20% likelihood) of accelerating a stable hemodynamically tolerated VT into an unstable VT or VF. Such failed ATP attempts may delay therapy, resulting in syncope, and lead to painful shock therapies.
A premature ventricular stimulation pulse for disrupting a ventricular tachycardia in the course of anti tachycardia pacing is considered safe if it is delivered during a window that is outside the VP. According to this invention, the timing of T wave is estimated from the preceding RR interval based on a programmed QT-RR relationship.
The QT-RR relationship has been extensively investigated during the past decades. It is well known that the QT interval is rate-dependent. In order to compare the QT interval recorded at different heart rates, effort has been made to estimate the heart-rate corrected QT interval (QTc), which relates the QT interval with the RR interval in a predefined mathematical formula, based on statistical regression analysis. Although dozens of QTc formulas have been proposed (linear model, hyperbolic model, parabolic model, etc.), controversial results on optimal regression parameters have been reported.
For the purpose of this disclosure, the following abbreviations are used are used:
TABLE 1AbbreviationMeaningApAtrial pace (stimulation) eventAsAtrial sense eventAAny atrial eventAVDAV delay as applied by the pacemaker (in contrast tointrinsic AV delay)ATPanti tachycardia pacingPVARPpost ventricular atrial refractory periodQTQT intervalQTccorrected QT intervalRRPeak-to-Peak interval between two consecutive R-wavesRTPeak-to-Peak interval between an R-wave and a T-wave ina same heart cycleRVpRight ventricular pacing interval for safe ATPVpVentricular pace (stimulation) eventVsVentricular sense eventVAny ventricular eventVTVentricular tachycardiaVFventricular fibrillation